21 - Heart Failure Flashcards
(43 cards)
1
Q
What is heart failure and what are the primary manifestations?
A
- Progressive clinical syndrome that can result from any changes in cardiac structure or function that impair ability of ventricle to fill or eject blood
- Primary manifestations = dyspnea, fatigue, fluid retention
2
Q
Cause of HF
A
- Abnormality in systolic function, diastolic function, or both
- Leading causes = coronary artery disease & HTN
3
Q
Major cause of death in people w/ HF?
A
- Sudden cardiac death (ventricular arrhythmia)
- Stable px are at risk across all stages of disease
4
Q
What is CO? What determines it?
A
- Amount of blood pumped out of left ventricle in 1 minute
- HR * SV
5
Q
What affects HR?
A
- Autonomic innervation
- Hormones
- Fitness levels
- Age
6
Q
What affects SV?
A
- Heart size
- Fitness levels
- Gender
- Contractility
- Duration of contraction
- Preload and afterload
7
Q
What is SV? What determines it?
A
- Volume ejected from ventricles in each beat
- EDV - ESV
- EDV = end diastolic volume
- ESV = end systolic volume
8
Q
What is preload? When is it increased?
A
- Volume of blood in ventricles at end of diastole (EDV)
- Increased in hypervolemia, regurgitation of cardiac valves, HF
9
Q
What is afterload? When is it increased?
A
- Resistance left ventricle must overcome to circulate blood
- Increased in HTN & vasoconstriction
10
Q
What is BP? What determines it?
A
- Measure of force being exerted on walls of arteries as blood is pumped out of heart
- SVR * CO
11
Q
What is SVR?
A
- Systemic vascular resistance
- Squeeze of the blood vessels outside the heart resisting blood flow
12
Q
What are the compensatory mechanisms in HF?
A
- Increased HR (symp activation) – one of the “first responders” to reduced CO
- Increased preload using RAAS (Na & H2O retention)
- Peripheral vasoconstriction
- Ventricular hypertrophy & remodeling (this is what really causes progression of the disease)
13
Q
Describe the Frank-Starling mechanism
A
Force of heart contraction is directly proportional to initial length of muscle fiber (w/in physiological limits); greater the stretch of the ventricular muscle, the more powerful the contraction is
14
Q
What are the neurohormonal factors involved in HF and what does each do?
A
- Angiotensin 2 – vasoconstriction, activates SNS, sodium retention, aldosterone release
- Norepi – tachycardia, vasoconstriction, increased contractility
- Aldosterone – RAAS sodium & water retention, contributes to ventricular remodeling
- Natriuretic peptides (atrial ANP, brain BNP) – BNP most important; both ANP & BNP increased in HF
- Arginine vasopressin (aka antidiuretic hormone ADH) – increases water retention, vasoconstriction, & contributes to ventricular remodeling
15
Q
What is the difference between myocardial and non-myocardial heart disease?
A
- Myocardial = ischemia, inflammation, dilated cardiomyopathy, familial; can be systolic and/or diastolic
- Non-myocardial = vascular (HTN), valvular (mitral/aortic insufficiency or stenosis), electric (A. fib, heart block), pericardial (tamponade, constriction)
16
Q
What are some precipitating factors that lead to acute decompensation?
A
- Increased circulating volume (increased preload) – high salt intake, noncompliance w/ fluid restriction or diuretics, NSAIDs, renal failure
- Conditions that increase afterload – uncontrolled HTN
- Conditions that impair contractility – MI, negative inotropic medications (diltiazem, verapamil)
- Increased metabolic demand – infection, pregnancy, anemia, hyperthyroidism, tachyarrhythmias
- Non-compliance w/ medications
- Bradyarrhythmias
17
Q
Describe ejection fraction
A
- % of blood ejected from heart w/ each contraction
- Normal ~ 60%
- EF < 40% referred to as HR w/ reduced left ventricular function (HRrEF) – systolic dysfunction
- EF >/ 40% referred to as HR w/ preserved left ventricular function (HFpEF) – diastolic dysfunction
18
Q
Signs and sx of HF
A
- Vasoconstriction -> decreased CO
- Increased HR -> increased oxygen utilization
- Increased preload -> peripheral & pulmonary edema
- Decreased exercise tolerance
- Pulmonary congestion (left sided) – exertional dyspnea, orthopnea (SOB when you lie down), paroxysmal nocturnal dyspnea, pulmonary edema
- Systemic congestion (right sided) – peripheral edema, jugular vein distention, organomegaly
- Low CO findings – fatigue, poor appetite, cold, pale clammy skin, altered mental status, resting tachycardia
19
Q
What is the difference between right sided and left sided HF?
A
- Right sided = blood backed up in abdominal organs & periphery
- Left sided = blood backed up in lungs
- Often occur simultaneously, or progresses to both left & right HF
20
Q
Describe the NYHA functional classes of HF
A
- Class 1 = able to perform ordinary physical activity
- Class 2 = ordinary physical activity results in sx
- Class 3 = less than ordinary physical activity results in sx
- Class 4 = sx may be present at rest
21
Q
What are some tests used to diagnose HF?
A
- EKG (electrocardiogram) may be normal or show numerous abnormalities (acute ST-T wave changes)
- Serum creatinine may be increased due to hypoperfusion
- Complete blood count used to see if HF due to reduced O2-carrying capacity
- Chest x-ray for detection of cardiac enlargement, pulmonary edema, & pleural effusions
- Echocardiogram to assess LV size, valve function, pericardial effusion, wall motion abnormalities, & EF
- Hyponatremia may indicate worsening volume overload and/or disease progression
22
Q
Goals of therapy for HF
A
- Minimize disabling sx
- Decrease hospitalization
- Improve QOL
- Minimize disease complications
- Slow progression of disease
- Improve survival
23
Q
Causes of decompensation/ exacerbation
A
- Cardiac events – MI, HTN
- Non-cardiac events – ex: pulmonary infections
- Non-adherence to meds or fluid/diet restriction
- Certain drugs – NSAIDs, DPP 4 inhibitor saxagliptin, thiazolidinediones (rosiglitazone, pioglitazone)
24
Q
Tx of HFrEF
A
- Must take off a CCB
- Triple therapy – ACEi/ARB, beta blocker & MRA to improve survival & reduce morbidity while improving functional capacity
- Reasses sx
- If NYHA1 – continue triple therapy
- If NYHA 2-4 and HR >/ 70 bpm – add ivabradine & swtich ACEi/ARB to ARNI for eligible px
- If NYHA 2-4 and HR < 70 bpm – switch ACEi/ARB to ARNI for eligible px
- Reassess sx & LVEF
- If NYHA 1 or LVEF > 35% – continue present management
- If NYHA 1-3 & LVEF /< 35% – refer to ICD/CRT algorithm
- If NYHA 4 – consider hydralazine/nitrates, referral to advanced HF therapy, or palliative care
25
What are some characteristics of HFpEF
- Diastolic HF
- Normal contractility & heart size
- Impaired LV filling during diastole
- LV stiffness & inability to relax during diastole
- Results in increased resting pressure w/in ventricle
- Increased pressure impedes ventricular filling, therefore reducing stroke volume (EF preserved)
- Focus on decreasing sx & addressing risk factors (ex: HTN, smoking)
- Treat comorbid conditions by controlling HR & BP, alleviating causes of myocardial ischemia, reducing volume, & restoring/maintaining sinus rhythm
26
Purpose of using ACE inhibitors for HF
- For HFrEF – improve survival, slow disease progression, reduce hospitalizations & improve QOL (most benefit at target doses)
- Hemodynamic effects – increase CO, decrease preload, systemic vascular resistance, & BP
- Hormonal effects (inhibit RAAS) – decrease angiotensin 2, aldosterone, & slow ventricular remodelling
- Indicated for all px w/ HFrEF along w/ BB & MRA
- Clinical pearl – introduce in graduated doses when pt is normovolemic or hypervolemic to avoid unnecessary hypotension or renal dysfunction
27
ACE inhibitors – adverse effects
- Hypotension – risk factors = stimulated RAAS, hyponatremia, diuretics, intravascular volume depletion
- Renal impairment
- Hyperkalemia (concurrent use w/ K+ sparing diuretics, MRAs, or K+ supplements)
- Cough
- Rash (more common w/ captopril)
- Taste alterations
- Angioedema (swelling of face, lips, tongue, larynx) – immediately d/c & don’t retry
28
ACE inhibitors – contraindications
- Hx of angioedema due to prior ACEi use
- Renal failure (creatinine > 220 umol/L)
- Bilateral renal artery stenosis
- High potassium (K+ > 5.5)
- Hypotension (cutoff is 80/50)
- Pregnancy
29
ACE inhibitors – monitoring
- Efficacy
- Right & left sided sx
- Exercise tolerance
- Weight/fluid balance
- Side effects
- Check renal function & electrolytes at baseline
- Monitor blood chemistry 1-2 weeks after dose initiation & 1-2 weeks after final dose titration, then monitor every 3-4 months thereafter
30
Effects of ARBs for HF
- Blocks AT1 receptor in vascular cardiac, brain, kidney, & adrenal gland tissue
- Candesartan shown to reduce CV mortality; valsartan shown to improve hospitalization rate due to HF
- Alternative if ACEi cough
- Combination w/ ACEi no longer recommended
- ADEs = similar to ACEi, less cough
31
Effects of beta blockers for HF
- Long term symp activation may contribute to disease progression, augmented activation of RAAS, peripheral vasoconstriction, & remodeling of cardiac myocytes
- Decrease all-cause mortality, sudden cardiac death, death due to worsening HF compared to placebo
- First line in addition to ACEi & MRA
- Indicated for all HFrEF (carvedilol, metoprolol, & bisoprolol)
- Start low, go slow to target doses (increase 50-100% every 2-4 weeks)
- Watch for fluid retention (weight gain) & monitor HR, BP, & EKG
32
Beta blockers – contraindications
- Acute decompensated HR/pulmonary congestion
| - Significant hypotension or bradycardia
33
Beta blockers – side effects
- Fatigue (improves after 3-6 weeks)
- Postural hypotension
- Fluid retention
- Cold extremities
34
Describe MRAs (mineralocorticoid receptor antagonist) for HF
- Reduce mortality in HFrEF (NYHA class 2-4 sx)
- Decrease risk of hospitalization in HFpEF
- Monitor potassium & renal function
- Should be considered as adjunctive therapy (ie already on ACEi & BB) in px w/ mild or moderate to severe HF (NYHA class 2-4)
- Rationale – aldosterone contributes to sodium/water retention, symp activation, myocardial & vascular fibrosis & other pathophysiologic effects seen in HF
- Spironolactone = aldosterone receptor antagonist, but also binds to androgen & progesterone receptors
- Eplerenone = selective aldosterone receptor antagonist; has greater selectivity for aldosterone receptor than spironolactone & therefore doesn’t lead to gynecomastia
35
Caution MRA use w/:
- Hyperkalemia (risk increases w/ concurrent use of ACEi or renal impairment)
- CI for px w/ sCr > 220 umol/L and/or K+ > 5 mmol/L
- Concurrent digoxin use (hyperkalemia may precipitate digoxin toxicity)
36
Describe use of diuretics for HF
- Sx control (peripheral edema or pulmonary congestion)
* Don’t improve survival
- Many px will need chronic diuretic therapy to maintain euvolemia after fluid overload is resolved
- Overdiuresis can lead to reduction in CO, renal perfusion, & sx of volume depletion
- Loop diuretics = more “efficient” diuresis
- Start w/ low dose & adjust to achieve daily body weight reduction of 0.75-1 kg until euvolemia
- Aim to maintain px on dry weight w/ lowest possible dose
37
Important notes about loop diuretics for HF
- Possible diuretic resistance (no weight loss despite increasing furosemide dose)
- - Add metolazone (usually given 30 min prior to furosemide); only used if at 120 mg furosemide
- - Try furosemide IV
- Metolazone – usual dose 2.5-10 mg/day; not used long-term, only for exacerbations
38
Diuretics – adverse effects & monitoring
- Volume depletion – leads to dehydration & reduction in BP & CO
- Check for signs of hypovolemia, symptomatic hypotension
- Loss of K+ & Mg (can induce or potentiate digoxin toxicity; aim to keep K+ over 4 mmol/L)
- Renal impairment (check sCr & BUN)
39
Describe hydralazine/ nitrate use for HF
- Significant reduction in mortality & improvement in exercise
- Most often used in px that can’t tolerate ACEi
- Sometimes used in combination w/ ACEi in black px b/c have less sensitivity to RAAS inhibition
- Rationale – vasodilation decreases cardiac work by overcoming detrimental effects of compensatory mechanisms; achieved through reduction of preload (nitrates) & afterload (hydralazine)
- Standard add-on for individuals of African descent
- All px can consider if ongoing sx w/ ACEi & BB or unable to tolerate neither ACEi nor ARB
40
Digoxin use for HF?
- Symptomatic benefits for HFrEF
- Improve QOL & reduce hospitalizations in px w/ symptomatic HF
- No mortality benefit
- Not first line (use after ACEi, BB, & MRA)
- Slows AV node conduction in A. fib & atrial flutter
- Increases vagal stimulation to SA node resulting in bradycardia
- Increases force & velocity of contraction through inhibition of Na/K/ATPase
- Factors affecting activity/toxicity – electrolyte disturbances (hypo & hyperkalemia) and renal function
41
What is entresto? What is it shown to improve? When is it used? Contraindications?
- ARNI (angiotensin 2 receptor blocker & neprilysin inhibitor) – combination necessary as inhibition of neprilysin leads to RAAS activation
- 1 trial showed reduction in all-cause mortality, CV mortality, & HF hospitalization rate; but higher reports of symptomatic hypotension & angioedema than enalapril alone
- May be considered as replacement for ACEi in px w/ HFrEF who remain symptomatic despite optimal tx w/ ACEi, BB, & MRA
- CI = hx of angioedema, hypotension, eGFR < 30 mL/min, K > 5.2 mmol/L
42
Describe lancora
- Generic = ivabradine
- Blocks I-f current in SA node that is responsible for controlling HR, which slows depolarization of sinus node & slows HR
- Doesn’t affect BP, myocardial contractility, or AV conduction
- Common SE = bradycardia, atrial fibrillation, visual disturbances
- CCS 2017 HF guideline = should be considered in px w/ HFrEF, who remain symptomatic despite tx w/ appropriate doses of GDMT w/ resting HR > 70 bpm & previous hospitalization w/in 12 months
43
Non-pharms for HF
- Exercise training
- Restriction of dietary sodium (< 2 g/day)
- Fluid restriction (< 1.5-2 L/day)
- Daily AM weights (w/o clothes & after voiding)
- Limit alcohol
- Quit smoking
- Look for & treat depression
